Risks for infection in patients with asthma (or other atopic conditions): is asthma more than a chronic airway disease?

Abstract

Most of the research effort regarding asthma has been devoted to its causes, therapy, and prognosis. There is also evidence that the presence of asthma can influence patients' susceptibility to infections, yet research in this aspect of asthma has been limited. There is additional debate in this field, with current literature tending to view the increased risk of infection among atopic patients as caused by opportunistic infections secondary to airway inflammation, especially in patients with severe atopic diseases. However, other evidence suggests that such risk and its underlying immune dysfunction might be a phenotypic or clinical feature of atopic conditions. This review argues (1) that improved understanding of the effects of asthma or other atopic conditions on the risk of microbial infections will bring important and new perspectives to clinical practice, research, and public health concerning atopic conditions and (2) that research efforts into the causes and effects of asthma must be juxtaposed because they are likely to guide each other.

Keywords: Adaptive immunity; allergic rhinitis; asthma; atopic dermatitis; epidemiology; immune dysfunction; immune incompetence; infection; innate immunity; phenotype; risk; susceptibility.

Figure 1

The relationship between microbial colonization or infections and atopic conditions. This diagram suggests a bidirectional causal relationship between exposure to microbial colonization or infection and risk of atopic conditions, which encompasses four specific hypotheses: the ‘hygiene hypothesis’, the ‘counter-hygiene hypothesis’, the ‘microbiome hypothesis’, and reverse causality. The ‘hygiene hypothesis’ suggests exposure to microbial colonization or infection during early childhood provides a protective effect on the development of atopic conditions whereas the ‘counter-hygiene hypothesis’ suggests a provocative effect of exposure to microbial infection during early childhood on the development of atopic conditions (eg, human rhinovirus infection). The recent microbiome hypothesis suggests a contextual effect of such exposure on the development of atopic conditions depending on diversity of microbiome. While these hypotheses address a causal direction for the influence of exposure to microbial organisms on the development of atopic conditions, reverse causality hypothesis argues for a causal direction that atopic conditions alter susceptibility to microbial colonization or infections.